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Module 103: The Heart, Lungs and Blood > Theme 3: Lecture 12 - Heart failure > Flashcards

Theme 3: Lecture 12 - Heart failure Flashcards

1
Q

Definition of heart failure

A

A state that develops when the heart fails to maintain an adequate cardiac output to meet the demands of the body

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2
Q

What is heart failure a result of

A

Results from any structural or functional abnormality that impairs the ability of the ventricle to eject blood (systolic HF) or fill with blood (diastolic HF)

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3
Q

What affects stoke volume

A
  • contractility
  • preload
  • afterload
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4
Q

In general, what does an increased heart rate result in

A

increased cardiac output

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5
Q

What does an excessively high heart rate result in

A

decrease in the amount of time allowed for the ventricles to fill in diastole which causes stroke volume and, thus cardiac output to fall

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6
Q

What is the typical cardiac output at rest

A

70mls/kg/min

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7
Q

What is contractility

A

the intrinsic ability of the myocardium to contract

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8
Q

What is preload

A

the volume of blood or stretching of cardiomyocytes at the end of diastole prior to the next contraction

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9
Q

What is afterload

A
  • the resistance/end load against which the ventricle contracts to eject blood
  • It is the pressure in the aorta/pulmonary artery that the left/right ventricular muscle must overcome to eject blood
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10
Q

What affects preload

A
  • Is affected by venous blood pressure and the rate of venous return to the heart
  • This, in turn, is affected by venous tone and volume of circulating blood
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11
Q

What causes an increase in preload

A

Preload increases with increasing blood volume and vasoconstriction

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12
Q

What causes a decrease in preload

A

Preload decreases with blood volume loss and vasodilatation

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13
Q

Describe the Frank Starling law

A
  • An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which, in turn, increases the stroke volume
  • Is true only up to a certain point… at some stage the fibres become over-stretched and the force of contraction is reduced
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14
Q

What causes an increase in afterload

A
  • The greater the aortic/pulmonary pressure, the greater the afterload on the left/right ventricle respectively
  • Afterload increase with hypertension and vasoconstriction
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15
Q

How does afterload affect cardiac output

A

As afterload increases, cardiac output decreases

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16
Q

Low output heart failure

A
  • Systolic heart failure

- Diastolic heart failure

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17
Q

High output heart failure

A
  • Occurs in the context of other medical conditions which increase demands on cardiac output, causing a clinical picture of HF
  • The heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one or more organs in the body
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18
Q

Which medical conditions cause high output heart failure (6)

A
  • thyrotoxicosis
  • profound anaemia
  • pregnancy
  • pagets disease
  • acromegaly
  • sepsis
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19
Q

What is thyrotoxicosis

A

overactive thyroid gland

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20
Q

What is Paget’s disease

A

Paget’s disease of bone is a chronic disease of the skeleton. In healthy bone, a process called remodeling removes old pieces of bone and replaces them with new, fresh bone. Paget’s disease causes this process to shift out of balance, resulting in new bone that is abnormally shaped, weak, and brittle.

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21
Q

What is acromegaly

A

Acromegaly is a disorder that results from excess growth hormone (GH) after the growth plates have closed. The initial symptom is typically enlargement of the hands and feet. There may also be an enlargement of the forehead, jaw, and nose

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22
Q

What is systolic heart failure

A

Progressive deterioration myocardial contractile function

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23
Q

What causes systolic heart failure

A
  • Ischaemic injury
  • Volume overload
  • Pressure overload
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24
Q

What is diastolic heart failure

A

Inability of the heart chamber to relax, expand and fill sufficiently during diastole to accommodate an adequate blood volume

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25
Q

What causes diastolic heart failure

A
  • Significant left ventricular hypertrophy (LVH) e.g HCM
  • Infiltrative disorders
  • Constrictive pericarditis
  • Restrictive cardiomyopathy
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26
Q

What are the causes of heart failure

A
  • Coronary Heart Disease
  • Hypertensive Heart Disease
  • Valvular Heart Disease
  • Myocardial Disease/ Cardiomyopathies
  • Congenital Heart Disease
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27
Q

Definition of cardiomyopathies

A

Diffuse disease of the heart muscle leading to functional impairment

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28
Q

What are the classes of cardiomyopathies

A
  • Dilated cardiomyopathy
  • Hypertrophic cardiomyopathy
  • Restrictive cardiomyopathy
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29
Q

Causes of dilated cardiomyopathy

A
  • various causes, 50% familial
  • ETOH
  • pregnancy
  • systemic disease (SLE)
  • muscular dystrophies
  • Drug toxicity
  • Myocarditis
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30
Q

What is myocarditis

A

Inflammation of the myocardium (heart muscle)

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31
Q

What are muscular dystrophies

A

Muscular dystrophy is a group of inherited diseases that damage and weaken your muscles over time.

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32
Q

Causes of hypertrophic cardiac myopathy

A

hereditary

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33
Q

Causes of restrictive cardiomyopathy

A

rare-amyloid the main cause in the UK

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34
Q

What is amyloid

A

A glycoprotein that is deposited in internal organs in amyloidosis

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35
Q

Describe the pathophysiology of heart failure

A

Pump failure leads to reduced SV and CO. Compensatory mechanisms kick in to maintain arterial pressure and perfusion of vital organs:

The Frank Starling mechanism: vasoconstriction, increased venous return to the heart, increased preload, heart muscle fibres stretch, enhanced contractility (initially beneficial but there is a limit beyond which this becomes unhelpful)

Myocardial structural change: Augmented muscle mass (hypertrophy) with or without cardiac chamber dilatation

Activation of neurohormonal system:

  • Release of Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
  • Release of ANP/BNP
  • Activation of renin-angiotensin – aldosterone system
36
Q

Describe the NP system

A
  • Distended ventricular wall leads to release of proBNP
  • proBNP is converted into either BNP or NT-proBNP
  • BNP is active and leads to diuresis, RAAS inhibition, SNS inhibition and vasodilation
  • NT-proBNP in non active but is used as a biomarker for heart failure
37
Q

What does NP stand for

A

Natriuretic peptide

38
Q

What does activation of the NP system lead to

A
  • Decreased BP
  • Decreased sympathetic tone
  • Decreased aldosterone levels
  • Natriuresis
  • Diuresis
  • Antifibrotic affects
39
Q

Describe what vasoconstriction does as a compensatory mechanism in heart failure

A

↑ resistance against which heart has to pump (i.e.↑afterload), and may therefore ↓ CO

40
Q

Describe what Na+ and water retention does an a compensatory mechanism in heart failure

A

↑fluid volume, which ↑ preload. If too much “stretch” → ↓ contractile strength and CO

41
Q

Describe what excessive tachycardia does as a compensatory mechanism in heart failure

A

↓diastolic filling time → ↓ventricular filling → ↓SV and CO

42
Q

What are the clinical types of heart failure

A
  • Left sided, right sided and biventricular failure
  • Acute and chronic heart failure
  • Compensated and decompensated heart failure
43
Q

What does left sided heart failure do

A

Backs up progressively from the left atrium to the pulmonary circulation

44
Q

Causes of left sided heart failure

A
  • Ischaemic heart disease
  • Hypertension
  • Valvular heart disease
  • Myocardial disease
45
Q

The symptoms of left sided heart failure due to the effect on the lungs

A
  • Pressure in the pulmonary veins is transmitted retrogradely to the capillaries and arteries
  • This leads to pulmonary congestion and oedema
  • Heavy wet lungs:
    • Breathlessness (dyspnoea) exaggeration of the normal breathlessness that follows exertion
    • Orthopnoea – breathlessness lying flat that is relieved by sitting or standing
    • Paroxysmal nocturnal dyspnoea – an extension of orthopnoea with attacks of extreme dyspnoea bordering on suffocation usually occuring at night
46
Q

The symptoms of left sided heart failure due to effect on the kidneys

A
  • Decreased cardiac output
  • Reduction in renal perfusion
  • Activation of renin - angiotensin – aldosterone system
  • Retention of salt and water with consequent expansion of interstitial fluid and blood volumes
47
Q

The symptoms of left sided heart failure due to effect on the brain

A
  • Hypoxic encephalopathy (brain disease/damage)
  • Irritability
  • Loss of attention
  • Restlessness
  • Stupor and coma
48
Q

Causes of right sided heart failure

A
  • Usually as a consequence of left sided heart failure (congestive cardiac failure (CCF))
  • Cor-pulmonale
  • Valvular heart disease
  • Congenital heart disease
49
Q

What is core pulmonale

A
  • Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
  • Usually as a result of respiratory disease e.g. COPD or pulmonary emboli
  • Normal left ventricular function
50
Q

Symptoms of right sided heart failure due to effect on the liver and portal system

A
  • Congestive hepatomegaly (enlarged liver)
  • Centrilobular necrosis when severe
  • Cardiac cirrhosis
51
Q

Symptoms of right sided heart failure do to the effect on the spleen

A

Congestive splenomegaly (enlargement of the spleen)

52
Q

Symptoms of right sided heart failure do to effect on the abdomen

A

Ascites

53
Q

Symptoms of right sided heart failure do to effect on the subcutaneous tissue

A
  • Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema
  • Sacral oedema if bedridden
54
Q

Symptoms of right sided heart failure do to effect on the pleural and pericardial space

A

effusions

55
Q

What causes biventricular heart failure (congestive cardiac failure)

A

-Either due to the same pathological process on each side of the heart
OR
-A consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure

56
Q

Clinical presentation on heart failure due to fluid accumulation

A
  • Dyspnoea
  • Orthopnoea, paroxysmal nocturnal dyspnoea
  • Oedema
  • Hepatic congestion
  • Ascites
57
Q

Clinical presentation of heart failure due to reduction in cardiac output

A
  • Fatigue

- Weakness

58
Q

New York Heart Association (NYHA) classification of heart failure

A
  • Class I: No limitation of physical activity
  • Class II: Slight limitation of ordinary activity
  • Class III: Marked limitation, even during less-than-ordinary activity
  • Class IV: Severe limitation with symptoms at rest
59
Q

Clinical signs of heart failure (9)

A
  • Cool, pale, cyanotic extremities
  • Tachycardia
  • Elevated JVP
  • Third heart sound (S3) – gallop rhythm
  • Displaced apex (LV enlargement)
  • Crackles or decreased breath sounds at bases on chest auscultation
  • Peripheral oedema
  • Ascites
  • Hepatomegaly
60
Q

Clinical tests for heart failure

A
  • CXR
  • ECG
  • Blood investigations
  • Echocardiogram / Cardiac MRI or CT / CT-PET
  • CTCA (CT coronary angiography) / Coronary angiography
61
Q

Name a loop diuretic

A

Frusemide

62
Q

Describe loop diuretics

A
  • Inhibit Na+ re-absorption from the proximal tubule
  • K+ loss from distal tubule
  • Can be given iv or orally
63
Q

Side effects of loop diuretics

A
  • electrolyte abnormalities

- hypovolaemia and diminished renal perfusion

64
Q

What is hypovolaemia

A

abnormally low extracellular fluid volume

65
Q

Name a mineralocorticoid receptor antagonist

A

Spironolactone

66
Q

Describe mineralocorticoid receptor antagonists (aldosterone antagonists)

A
  • antagonizes the action of aldosterone at mineralocorticoid receptors
  • Acts on distal tubule
  • Promotes Na+ excretion and K+ re-absorption
  • Reduces hypertrophy and fibrosis
67
Q

Side effects of mineralocorticoid receptor antagonists (aldosterone antagonists)

A
  • Gynaecomastia (esp. Spironolactone)

- Electrolyte (K+ high) and renal function abnormalities

68
Q

What is gynaecomastia

A

males develop breast tissue

69
Q

Name an ACE inhibitor

A

Ramipril

70
Q

Describe ACE inhibitors

A
  • Act on activated renin - angiotensin system
  • Given orally in small doses with slow titration
  • Block production of angiotensin:
    • Vasodilatation
    • BP lowering
    • Reduce cardiac work
71
Q

Side effects of ACE inhibitors

A
  • Cough
  • Hypotension
  • Renal impairment
72
Q

Name a beta blocker

A

bisoprolol

73
Q

Describe beta blockers

A
  • Block the action of adrenaline and noradrenaline on adrenergic beta receptors
  • Slow HR, reduce BP
  • Given orally in small doses with slow titration
  • (treat arrhythmias)
74
Q

Side effects of beta blockers

A
  • Bronchospasm

- Claudication

75
Q

What is claudication

A

pain and/or cramping in the lower leg due to inadequate blood flow to the muscles

76
Q

Name an SA node blocker

A

Ivabradine

77
Q

Describe ivabradine

A
  • Blocks the If channel within the SA node
  • Slow HR, no effect on BP
  • Given orally with dose titration
78
Q

Side effects of ivabradine

A
  • Visual aura

- Bradycardia

79
Q

Describe digoxin

A
  • Increases myocardial contractility
  • Slows conduction at the AV node (use in AF)
  • Excreted by kidney - Toxicity important
80
Q

When is digoxin given

A
  • Acute HF especially in AF

- Chronic HF in selected cases

81
Q

Describe Angiotensin receptor neprilysin inhibitors (ARNI)

A
  • Acts on activated renin - angiotensin system
  • Also blocks breakdown of ANP/BNP
  • Block production of angiotensin: (Vasodilatation, BP lowering, reduce cardiac work)
  • Promote natriuresis: (Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis)
82
Q

Side effects of Angiotensin receptor neprilysin inhibitors

A
  • Hypotension

- Renal impairment

83
Q

What is neprilysin

A

A protein that breaks NPs down into inactive fragments among other things

84
Q

Non drug therapies for heart failure (7)

A
  • Cardiac Resynchronisation Therapy (CRT)
  • Implantable Cardioverter Defibrillator (ICD)
  • Dialysis & Ultrafiltration
  • Ventricular Assist Device (LVAD/RVAD)
  • Intra-aortic balloon pump
  • Cardiac transplantation
  • (Stem cell therapy)
85
Q

Describe cardiac resynchronisation therapy AKA biventricular pacing

A
  • Standard pacemakers equipped with two wires (or “leads”) conduct pacing signals to specific regions of heart
  • Biventricular pacemakers have an additional third lead designed to conduct signals directly into the left ventricle
  • Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.

Module 103: The Heart, Lungs and Blood (51 decks)

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